ReferenceID 1586
Corylin Inhibits Vascular Cell Inflammation, Proliferation and Migration and Reduces Atherosclerosis in ApoE-Deficient Mice
Antioxidants (Basel)
Atherosclerosis is a complex disease that includes several events, including reactive oxygen species (ROS) stress, inflammation, endothelial dysfunction, lipid deposition, and vascular smooth muscle cell (VSMC) prolifera
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- Reference Id
- 1586
- Evidence Id
- 18176
- Core Evidence Id
- 18176
- Source Reference Id
- 3182
- Herb2 Reference Id
- HBREF003979
- Subject Paper Key
- HBIN021561_32218307
- Pubmed Id
- 32218307
- Doi
- 10.3390/antiox9040275
- Paper Title
- Corylin Inhibits Vascular Cell Inflammation, Proliferation and Migration and Reduces Atherosclerosis in ApoE-Deficient Mice
- Paper Abstract
- Atherosclerosis is a complex disease that includes several events, including reactive oxygen species (ROS) stress, inflammation, endothelial dysfunction, lipid deposition, and vascular smooth muscle cell (VSMC) proliferation and migration, which result in atherosclerotic plaque formation. Corylin, a flavonoid compound, is known to exhibit antioxidative, anti-inflammatory and antiproliferative effects. However, it remains unknown whether corylin could modulate atherogenesis. Here, we identified the anti-inflammatory effect of corylin in tumor necrosis factor-alpha (TNF-alpha)-induced vascular cells. In human umbilical vein endothelial cells (HUVECs), corylin suppressed TNF-alpha-induced monocyte adhesion to the HUVECs and transmigration by downregulating the ROS/JNK/nuclear factor-kappa beta (NF-kappaB) p65 pathway. In VSMCs, corylin inhibited TNF-alpha-induced monocyte adhesion by suppressing ROS production, mitogen-activated protein kinase (MAPK) phosphorylation and NF-kappaB p65 translocation. In platelet-derived growth factor-BB (PDGF-BB)-induced VSMCs, corylin inhibited PDGF-BB-induced VSMC proliferation and migration through regulating the mammalian target of rapamycin (mTOR)/dynamin-1-like protein 1 (Drp1) signaling cascade. In addition, corylin treatment not only attenuated atherosclerotic lesions, ROS production, vascular cell adhesion protein-1 (VCAM-1) expression, monocyte adhesion and VSMC proliferation in apolipoprotein E (ApoE)-deficient mice but also inhibited neointimal hyperplasia in endothelial-denuded mice. Thus, corylin may be a potential prevention and treatment for atherosclerosis.
- Journal
- Antioxidants (Basel)
- Publish Year
- 2020
- Experiment Subject
- mouse; human; human umbilical vein endothelial cells; huvecs; platelet-derived growth factor-bb (pdgf-bb)-induced vsmcs; tumor necrosis factor-alpha (tnf-alpha)-induced vascular cells
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Atherosclerotic Lesions; Inflammation; Tumor; Endothelial Dysfunction; Neointimal Hyperplasia; Atherosclerosis
- Paper Title Cn
- Paper Title En
- Corylin Inhibits Vascular Cell Inflammation, Proliferation and Migration and Reduces Atherosclerosis in ApoE-Deficient Mice
- Bilingual Status
- semi_complete